The process of scientific research is never as smooth and linear as one would hope. What starts out as a simple and straightforward experimental setup can be plagued with errors and endless troubleshooting. I began this summer’s research with the goal of determining whether acetone is the environmental stimulus that triggers the activation of the CrdRS signal transduction pathway in H. pylori (HP). The experimental design is simple: I grow up some HP cells in blood agar plates, pass them to SFBB culture after 24 hours, treat one group with acetone, extract RNA from the resulting cell pellets, turn the RNA into cDNA, and run a qRT-PCR with the cDNA samples. I was hoping to get some sort of data by the end of the first week. But such was not the case in reality.

My name is Yusheng Qin. I’m a rising Junior and a Biology major at the College of William and Mary. For the past year, I’ve been working in Dr. Mark Forsyth’s lab on signal transduction in Helicobacter pylori. H. pylori (HP) is a bacterium that causes many gastric diseases in humans such as gastric ulcers and gastric cancers. In order to thrive in the highly acidic environment in the stomach, HP has evolved complex mechanisms for resistance to environmental changes in the stomach such as pH fluctuations. One way the gastric pathogen achieve this is through the use of two-component signal transduction (TCST) systems. This summer I will be studying one of these TCST systems named CrdRS.